Helicobacter pylori and increased epithelial cell proliferation

Cahill, Rachel; Sant, S.; Beattie, S.; Hamilton, H.; O’Moráin, Colm

doi:10.1097/00042737-199412000-00010

Cited by 46 publications

(32 citation statements)

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“…Increased cell proliferation has been identified as an underlying mechanism for increased mutagenesis, and possibly initiates carcinogenesis (Ames and Gold, 1990;Eidt et al, 1995); it has also been thought to be a consequence of chronic H. pylori infection (Cahill et al, 1994;Correa et al, 1994). As measuring mucosal proliferation is complicated and time-consuming, replacement of the surface epithelium by regenerative epithelium (RE) can be assessed instead, because this parameter is closely correlated with the grade of epithelial proliferation (Stolte et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Miehlke

Hackelsberger²,

Meining³

et al. 1998

Br J Cancer

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Summary In 50 Helicobacterpylori-infected gastric carcinoma patients the corpus gastritis was significantly higher than in matched H. pyloripositive control subjects (P < 0.01). Atrophy and intestinal metaplasia (IM) occurred significantly more often in the antrum of carcinoma patients (P < 0.01). The odds ratio for gastric carcinoma was 8.85 for high-grade corpus gastritis and 8.04 when atrophy in the antrum was present.

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Section: Discussionmentioning

confidence: 99%

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Miehlke

Hackelsberger²,

Meining³

et al. 1998

Br J Cancer

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“…pylori-induced inflammatory response may contribute to gastric carcinogenesis by increasing the rate of epithelial cell proliferation, [38][39][40][41][42] by damaging mucus secretion, 43 and by induction of mutations through a release of active oxygen and nitrogen species (oxygen radicals, nitric oxide) by polymorphonuclear cells and macrophages attracted by the bacteria. [44][45][46][47] For example, local production of tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-6 have been demonstrated to occur in H. pylori gastritis.…”

Section: Inflammatory Reaction and Factors In Host Responsementioning

confidence: 99%

Pathogenesis of the transformation from gastritis to malignancy

Sipponen¹,

Hyvärinen

Seppälä

et al. 1998

Aliment Pharmacol Ther

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cause of chronic gastritis, and on the knowledge of the natural course of chronic gastritis from non-atrophic gastritis to atrophic gastritis and intestinal metaplasia, and to precancerous lesions ( Figure 1). Prospective cohort studies are also considered to indicate strongly an association of H. pylori infection with gastric cancer. 1Our knowledge of the global epidemiology and time trends of gastric cancer indicates the importance of environmental factors in cancer pathogenesis. The timerelated changes in gastric cancer incidence have been substantial over the years but these changes are surprisingly similar worldwide, suggesting that one or some environmental agents play a critical role globally in gastric carcinogenesis.

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“…Prototypically, Helicobacter pylori has been linked to mutagenic free radical formation leading to chronic gastric inflammation and the stimulation of cellular proliferation (2)(3)(4). Mechanisms for H. pylori-induced cellular proliferation and carcinogenesis are under active investigation, but other model systems for complex interactions between bacterial pathogens and host responses, resulting in the development of cellular proliferation and the cancer phenotype are not well described.…”

mentioning

confidence: 99%

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

Preciado

Caicedo

Jhanjee

et al. 2005

The Journal of Immunology

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NF-κB is activated during acute inflammatory states as well as in other injury response disease states. Several pathologic states in squamous tissue injury response are characterized by increased squamous proliferation. This study was performed to investigate the hypothesis that Pseudomonas aeruginosa LPS is able to activate a proliferative phenotype in squamous cells via NF-κB induction and that this NF-κB-mediated response may be abrogated with the classic anti-inflammatory agent indomethacin. EMSA, luciferase reporter gene experiments, Western blots, and cellular proliferation assays were performed in normal and transformed human keratinocytes after stimulation with P. aeruginosa LPS. EMSA and luciferase reporter gene assays showed a 3- to 5-fold induction of active NF-κB in human keratinocyte cell lines after stimulation with P. aeruginosa LPS. The stimulation correlated with significantly increased cellular proliferation. As one potential mechanism for this increase in proliferation, an NF-κB-specific activation of cyclin D1 was observed. Both the NF-κB induction and proliferation response were inhibited with indomethacin and in dominant negative stable transfection clones. P. aeruginosa LPS activates proliferation of human keratinocytes, potentially through the induction of NF-κB and cyclin D1. These findings suggest that bacterial components can contribute to proliferative disease states in squamous epithelium through NF-κB activation.

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Helicobacter pylori and increased epithelial cell proliferation

Cited by 46 publications

References 0 publications

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Pathogenesis of the transformation from gastritis to malignancy

Pseudomonas aeruginosaLipopolysaccharide Induction of Keratinocyte Proliferation, NF-κB, and Cyclin D1 Is Inhibited by Indomethacin

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